目的 探究咪达唑仑诱导宫颈癌细胞铁死亡的作用与机制。方法 体外培养人宫颈癌 HeLa 细胞，将其分为 5 个组，L⁃咪达唑仑组/M⁃咪达唑仑组/H⁃咪达唑仑组分别注入 5、10、20 μmol/L 咪达唑仑、高剂量咪达唑仑+核因子 E2 相关因子 2 激活剂组注入 20 μmol/L 咪达唑仑和 80 nmol/L Bardoxolone、另设正常培养的 HeLa 细胞为 Control 组，继续培养 24 h。采用 CCK⁃8、克隆形成实验检测细胞增殖；PI 染色检测细胞死亡率；透射电镜观察线粒体形态变化；试剂盒检测铁、活性氧（ROS）、谷胱甘肽（GSH）、丙二醛 （MDA）水平；Western blot 检测 Nrf2/血红素氧合酶⁃1（HO ⁃1）信号通路相关蛋白及 GSH 过氧化物酶 4 （GPX4）蛋白表达情况。结果 与 Control 组比较，L⁃咪达唑仑组、M⁃咪达唑仑组、H⁃咪达唑仑组 HeLa 细胞 活力下降，克隆数减少，细胞死亡率增加，线粒体呈现显著铁死亡特征，细胞中铁、ROS、MDA 水平升高， GSH水平及GPX4、核Nrf2、HO⁃1蛋白表达下降，且H⁃咪达唑仑组变化更明显（P < 0.05）。与H⁃咪达唑仑组 比较，H⁃咪达唑仑+Nrf2激活剂组HeLa 细胞活力升高，克隆数增加，细胞死亡率减少，线粒体铁死亡损伤程 度减轻，细胞中铁、ROS、MDA水平下降，GSH水平及GPX4、Nrf2、HO⁃1蛋白表达升高（P < 0.05）。结论 咪达 唑仑能以剂量依赖性方式抑制HeLa细胞增殖，诱导其铁死亡，可能通过抑制Nrf2/HO⁃1信号通路实现。 

Objective To explore the effect and mechanism of midazolam inducing ferroptosis in cervical cancer cells. Methods Human cervical cancer HeLa cells were cultured in vitro and divided into 5 groups. Low/ medium/high dose midazolam groups were injected with 5 doses，respectively 5，10，20 μmol/L midazolam，high⁃ dose midazolam+nuclear factor E2 related factor 2 activator group injected with 20 μmol/L midazolam and 80 nmol/L Bardoxolone，as well as normal cultured HeLa cells，were used as control groups for further cultivation for 24 hours. CCK⁃8 and clone formation assay were used to detect cell proliferation；PI staining was used to detect cell death； transmission electron microscopy was used to observe mitochondrial morphological changes ；kits were used to detect the levels of iron，reactive oxygen species（ROS），glutathione（GSH），malondialdehyde（MDA）；Western Blot was used to detect the protein expressions of Nrf2/heme oxygenase⁃1（HO⁃1）signaling pathway⁃related proteins and GSH peroxidase 4（GPX4）. Results Compared with the Control group，the L⁃midazolam group，M⁃midazolam group，and H⁃midazolam group showed a decrease in HeLa cell viability，a decrease in clone count，an increase in cell mortality，and a significant ferroptosis feature in mitochondria. The levels of iron，ROS，and MDA in cells increased，while GSH levels and GPX4，nuclear Nrf2，and HO⁃1 protein expression decreased. The H⁃midazolam group showed more significant changes（P < 0.05）. Compared with the H ⁃midazolam group，the H ⁃midazolam+ Nrf2 activator group showed an increase in HeLa cell viability，increased clone count，decreased cell mortality， reduced mitochondrial iron death damage，decreased levels of iron，ROS，and MDA in cells，and increased levels of GSH and GPX4，Nrf2，and HO⁃1 protein expression（P < 0.05）. Conclusion Midazolam can inhibit the prolif⁃ eration of HeLa cells and induce ferroptosis in a dose dependent manner，which may be achieved by inhibiting the Nrf2/HO⁃1 signaling pathway.